BACKGROUND Over 5000 plant species produce milky latex sap utilized in decoration and various industries. Sap exposure, however, can elicit toxic reactions, including acute keratoconjunctivitis and corneal stromal infiltration. The common ornamental plant Dieffenbachia can cause acute keratoconjunctivitis and the deposition of fine blue crystals within the corneal stroma. This report analyzes 3 cases of Dieffenbachia-induced keratitis and reviews existing literature on plant-induced keratitis. CASE REPORT Three patients presented with ocular irritation, pain, and redness following accidental exposure to Dieffenbachia sap. Clinical examination revealed chemosis and corneal edema in all cases. Slit-lamp microscopy identified fine, needle-like oxalate crystals located within the epithelial and stromal layers of the inferior cornea. The 3 patients received conservative management: ocular irrigation, topical antibiotics, and localized anti-inflammatory agents. The treatment protocol was altered, depending on the clinical ocular response. When symptoms gradual improved, anti-inflammatory medication was decreased by 1 to 2 doses after 1 to 2 weeks, throughout a treatment duration of 4 to 8 weeks. Complete resolution of crystal deposits in the cornea was observed after a 4- to 8-week follow-up period. All patients retained satisfactory visual acuity and exhibited no corneal opacities. CONCLUSIONS Patients with keratitis caused by Dieffenbachia sap typically achieve full recovery without complications, but the potential for crystal deposition in the cornea must be recognized. Safety measures, including protective eyewear, gloves, and long-sleeved clothing during plant maintenance are essential. Comprehensive knowledge of the pathogenesis and clinical trajectory of ocular Dieffenbachia exposure will enable ophthalmologists to optimize treatment strategies.

Vasculitic skin lesions have been reported in association with both SARS-CoV-2 infection and vaccination. Whether viral proteins persist in lesional vessels beyond the acute phase remains unclear. The aim of this study was to investigate the presence of SARS-CoV-2 spike protein in persistent or delayed-onset cutaneous vasculitis temporally associated with COVID-19 infection or vaccination. This retrospective case-control study includes 9 patients with persistent or delayed-onset vasculitic skin lesions following COVID-19 infection (n=4) or mRNA vaccination (n=5). Skin biopsies were analysed using immunofluorescence for SARS-CoV-2 spike protein. Prepandemic leukocytoclastic vasculitis (n=3) and healthy postinfection/postvaccination skin (n=3) served as controls. Spike protein was detected in vascular endothelial cells of all 9 patients with COVID-19- or vaccine-associated vasculitis. Staining was absent in all prepandemic vasculitis and healthy control samples. Histopathology showed typical features of leukocytoclastic vasculitis without evidence of viral cytopathic changes. We found that SARS-CoV-2 spike protein can persist in endothelial cells of vasculitic skin lesions weeks to months after COVID-19 infection or mRNA vaccination. These findings suggest that retained viral proteins may contribute to prolonged or delayed-onset vasculitic skin manifestations. Further studies are needed to clarify the mechanisms underlying spike persistence and its clinical significance.

Acute hemorrhagic edema of infancy (AHEI) is a rare leukocytoclastic vasculitis of young children characterized by cockade-like purpura and edema, usually with a preserved general condition. Because of its dramatic presentation, it may mimic life-threatening disorders such as meningococcemia with purpura fulminans, leading to extensive investigations and unnecessary treatment. We report two cases of AHEI in boys aged 18 and 22 months. The first presented with widespread purpura after a recent fever, prompting a full sepsis workup and empirical ceftriaxone before AHEI was recognized. The second had typical cockade purpura with acral edema and no fever, allowing immediate diagnosis and simple clinical monitoring. Both children recovered spontaneously, with complete resolution within 10-14 days. Early recognition of AHEI is essential to avoid misdiagnosis and to adjust management appropriately in infants presenting with purpura.

Mendelian susceptibility to mycobacterial disease (MSMD), caused by IL12RB1 or IL12B mutations, typically presents with intra-cellular infections such as BCG-adenitis or Salmonella. Rarely, patients with IL12RB1/IL12B defects can exhibit cutaneous manifestations such as Henoch-Schonlein purpura (HSP). This study aimed to evaluate such vasculitic manifestations in genetically confirmed cases with MSMD in India and review the literature for similar associations. We included nine patients with genetically proven MSMD presenting with features of HSP-like small vessel vasculitis from pediatric immunology clinics across three tertiary care centers in India. Clinical, laboratory, histopathological, and genetic data were recorded using a structured proforma. Skin biopsy findings, IgA levels, renal involvement, and infection history were analyzed. Additionally, a literature review was performed using PubMed, Scopus, and Google Scholar databases to identify similar reported cases. In our cohort, eight patients had IL12RB1 defect, and one had IL12B defect. All had maculopapular purpuric rash in lower limbs, predominantly in the anterior aspect of legs and posterior thighs resembling the rash of HSP. Leukocytoclastic vasculitis was observed in 77.7% patients (n = 7), with two out of five had IgA deposits in dermo-epidermal junction. Concurrent infections due to Salmonella sp. and Pandorea apista were documented in 44.4% (n = 4) and 22.2% (n = 2), respectively. Treatment focused on antimicrobial therapy led to clinical improvement. The HSP-like vasculitic rash usually occurred in setting of underlying bacterial infections in patients with particularly IL12RB1/IL12B defects. These skin lesions can also be considered as one of the potential clinical clues for underlying IL12RB/IL12B defects.

A man in his 50s receiving immunomodulatory therapy for presumed Behçet's disease presented with odynophagia and jaw pain. Three months earlier, he had developed deep vein thrombosis and extensive superficial phlebitis with transmural inflammation on histopathology. Imaging revealed carotid artery vasculitis and unilateral inflammation around the temporal vessels. Ultrasound demonstrated wall thickening of the right temporal vein with normal temporal arteries. Persistent systemic inflammation and bicytopenia prompted bone marrow examination revealing myelodysplastic syndrome. Detection of a somatic UBA1 mutation confirmed VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic). Glucocorticoids and interleukin-1 blockade were initiated. Due to severe cytopenia, the patient underwent allogeneic haematopoietic stem cell transplantation, resulting in clinical remission. VEXAS causes variable vessel vasculitis, affecting arteries and veins alike even without thrombosis. In older men with myelodysplasia or cytopenia, VEXAS should be considered in the differential of both venous and arterial vasculitis. Ultrasound may distinguish temporal phlebitis from giant cell arteritis.

Immunoglobulin A vasculitis is uncommon in adults and is frequently associated with an identifiable trigger, most often infection. Invasive meningococcal disease is a rare but life-threatening infection caused by Neisseria meningitidis. We report the case of an 18-year-old Indigenous Australian woman who presented with fever, purpuric rash, ankle synovitis, abdominal pain, and systemic inflammation. A skin biopsy demonstrated leukocytoclastic vasculitis with immunoglobulin A deposition on immunohistochemistry, and blood cultures subsequently identified N. meningitidis serogroup B. Cerebrospinal fluid studies were unremarkable. The patient was treated with intravenous ceftriaxone, with complete clinical resolution and no recurrence at a 6-month follow-up. This case highlights a previously unreported association between immunoglobulin A vasculitis and invasive meningococcal disease in an adult patient, and it expands the spectrum of infectious triggers associated with adult-onset immunoglobulin A vasculitis.

We report a case of leukocytoclastic vasculitis (LCV) in a 74-year-old woman, occurring seven months after the initiation of fluoxetine therapy for generalized anxiety disorder (GAD). The cutaneous lesions resolved upon discontinuation of fluoxetine but recurred promptly upon rechallenge. Notably, subsequent exposure to paroxetine, another selective serotonin reuptake inhibitor (SSRI) previously tolerated by the patient, also elicited a similar but less severe rash, suggesting cross-sensitization. Transition to venlafaxine, a serotonin-norepinephrine reuptake inhibitor (SNRI), led to complete and sustained resolution of the skin lesions. This case highlights three key clinical points: the potential for delayed-onset cutaneous adverse reactions to SSRIs even after months of uneventful treatment; the occurrence of cross-reactive hypersensitivity among SSRIs; and the importance of considering alternative antidepressant classes with distinct pharmacological profiles in patients with SSRI-associated vasculitis.

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare, potentially life-threatening immune-related adverse event that can be triggered by immune checkpoint inhibitors. We present the case of a 58-year-old woman with malignant acral melanoma who developed late-onset DRESS following sequential treatment with pembrolizumab and nivolumab. The patient initially developed a generalized erythrodermic, scaly rash with pruritus after the third dose of pembrolizumab, which recurred upon switching to nivolumab. Laboratory evaluation revealed leukocytosis, marked eosinophilia, transaminitis, and elevated lactate dehydrogenase. Skin biopsies demonstrated spongiosis, basal vacuolar degeneration, eosinophilic infiltrate, and leukocytoclastic vasculitis, consistent with DRESS. Despite corticosteroid therapy, the patient experienced multiple relapses triggered by immunosuppressant tapering, requiring prolonged cyclosporine treatment. Her presentation met the registry of severe cutaneous adverse reactions (RegiSCAR) criteria for definite DRESS. This case underscores the need for heightened awareness of delayed hypersensitivity reactions to immune checkpoint inhibitors and highlights the possibility of a chronic-relapsing course requiring extended immunosuppressive therapy.

Our manuscript presents a rare case of idiopathic mesenteric phlebosclerosis (IMP) in a 73-year-old woman who experienced recurrent abdominal pain and diarrhea. Through a detailed clinical investigation, including laboratory tests, colonoscopy, biopsy, and enhanced abdominal CTA, we diagnosed the patient with IMP. Notably, we identified a potential link between the patient's long-term intake of a traditional Chinese herb containing Gardenia Fructus and the development of IMP. This finding is supported by existing literature, which suggests that genipin, a component of Gardenia Fructus, may cause intimal hyperplasia and fibrosis of the venous wall, leading to chronic intestinal ischemia. Our case highlights the importance of considering herbal intake as a potential risk factor for IMP and underscores the need for clinicians to be aware of the potential adverse effects of traditional herbal remedies.

Angiotensin-converting enzyme (ACE) inhibitor-associated hypersensitivity vasculitis with gastrointestinal involvement is an uncommon but important drug-related cause of acute abdominal pain and may mimic an acute surgical abdomen. We report the case of an 84-year-old man admitted for redo aortic valve replacement following infective endocarditis, who developed acute abdominal pain on postoperative day 14. Physical examination revealed diffuse abdominal tenderness and cutaneous purpura. Laboratory testing showed elevated inflammatory markers with peripheral eosinophilia. Contrast-enhanced abdominal CT demonstrated concentric small bowel wall thickening with submucosal edema and ascites, without evidence of mesenteric ischemia. Skin biopsy confirmed leukocytoclastic vasculitis. Lisinopril was initiated at the time of admission and continued throughout the perioperative period; symptoms occurred approximately three weeks after treatment initiation, with no prior history of similar episodes. Discontinuation of lisinopril resulted in rapid clinical improvement and complete resolution of abdominal symptoms. This case highlights that ACE inhibitor-associated hypersensitivity vasculitis may present with small bowel edema and imaging findings overlapping with intestinal angioedema. Careful medication review and recognition of associated systemic features such as purpura and eosinophilia are essential to avoid unnecessary invasive procedures.

Cite this article as: Günegül Y, Tozlu M, Demiral YE, Eminler AT, Uslan Mİ. Leukocytoclastic vasculitis occurring during upadacitinib therapy in ulcerative colitis: A case report. Turk J Gastroenterol. 2026;37(4):529-531.

BACKGROUND Dalbavancin is a lipoglycopeptide antibiotic largely used to treat serious and complex bacterial infections, particularly those caused by gram-positive bacteria. Its main advantages include a prolonged half-life, which allows for once-weekly dosing, effectiveness against resistant pathogens, most notably, methicillin-resistant Staphylococcus aureus, and a good profile of tolerability and patient adherence. Herein we report the first documented case of a patient who developed palpable purpura on both lower limbs following treatment with dalbavancin, which was clinically and histologically diagnosed as leukocytoclastic vasculitis (LV). CASE REPORT A 66-year-old woman received dalbavancin due to an acute bacterial skin and skin structure infection (ABSSSI) of her right leg. The patient initially showed a favorable clinical response, with marked improvement of the infection. However, 3 weeks after the administration of dalbavancin, she developed a diffuse erythematous palpable purpura, predominantly affecting the lower limbs, and accompanied by mild arthralgia and generalized asthenia. To further investigate and confirm the underlying cause of these new symptoms, a skin biopsy was performed, revealing histopathological findings consistent with LV. Following the diagnosis, corticosteroid therapy was initiated, resulting in a significant symptomatic improvement. CONCLUSIONS To the best of our knowledge, this is the first published, histologically confirmed case report of LV developing after treatment with dalbavancin. Given the widespread use of dalbavancin for treating ABSSSIs, clinicians should be aware of the potential adverse effects, including LV, that may arise during its administration.

Leukocytoclastic vasculitis (LCV) is a disease secondary to infections, malignancies, or drug exposure, although its pathogenesis remains unclear. Secondary LCV from different causes in the same patient has been rarely reported. We present a case of LCV secondary to pancreatic cancer that remained in remission for one year post-surgery, after which the patient suffered from a subdiaphragmatic abscess caused by Escherichia coli, followed by recurrence of LCV. This case suggests that patients with acquired hyposplenism may be susceptible to developing LCV as a manifestation of underlying disease. Careful evaluation of the underlying disease is important to avoid inappropriate immunosuppressive treatment.

Vancomycin is a first-line antibiotic used for severe gram-positive infections, but it may rarely trigger immune-mediated small-vessel vasculitis. We report a case of a 43-year-old man with end-stage renal disease on home hemodialysis who developed palpable purpuric skin lesions three days after starting vancomycin for L5-S1 discitis and osteomyelitis. Over the following days, the eruption progressed into symmetric, non-blanching purpuric plaques involving the upper and lower extremities by day 6 of therapy. Laboratory evaluation demonstrated progressive thrombocytopenia, an increase in eosinophil counts within the normal reference range, and elevated inflammatory markers, which declined after vancomycin cessation. Vancomycin was discontinued, and antimicrobial therapy was transitioned to daptomycin, resulting in rapid clinical improvement within 48 hours and near-complete resolution by day 12. This case emphasizes the importance of early recognition of vancomycin-induced leukocytoclastic vasculitis, particularly in patients with renal impairment who may experience an accelerated onset. Prompt discontinuation of the offending agent typically results in rapid recovery without the need for systemic corticosteroids.